The smooth muscle cell is a major muscle cell in tissues such as blood vessel, trachea, digestive tract, urinary bladder, and uterus, and its important function is the regulation of contraction and relaxation. Recently, a relationship has been revealed between phenotypic modulation of the smooth muscle cells, wherein the cell looses the contraction ability and thereby acquires proliferation ability, and the pathological state. The proliferation of vascular smooth muscle cell is closely associated with the manifestation of the pathological state such as restenosis occurring after percutaneous transluminal coronary angioplasty (PTCA). It has been clarified that vascular tunica media smooth muscle cells acquire motility through phenotypic modulation to a dedifferentiated type in the early stage of the onset of arteriosclerosis, and thus, migrate to the vascular endothelium, which is the major cause of hypertrophy of vascular endothelium. However, there are still many obscure points about the phenotypic modulation of smooth muscle cells, for example, associated genes, molecular mechanism thereof, and so on. A better understanding of how the smooth muscle cells maintain the differentiated phenotype and how their phenotypes are converted to the dedifferentiated type is needed to develop therapeutic methods for morbid states caused by smooth muscle cell proliferation. The mechanism of the phenotypic modulation may be elucidated by analyzing the genes associated with the maintenance of differentiated type of smooth muscle cells, such genes being applicable as therapeutic agents and diagnostic agents for diseases caused by the aberrant proliferation of smooth muscle cells; ischemic heart diseases such as arteriosclerosis, myocardial infarction, aortic aneurysm, and cerebral apoplexy; cerebral vascular disorders; and vascular dementia. In addition, glomerulonephritis, pulmonary fibrosis, cerebral arteriosclerosis, and hepatitis, which correspond to a state of aberrant proliferation of mesangial cells, alveolar epithelial cells, pericytes, and Ito cells, respectively—cells that have extremely similar characteristics to the smooth muscle cells—are presumed to be diseases caused by cellular transformation occurring through a mechanism similar to that of smooth muscle cells; and thus, the genes therein may also be applicable as therapeutic agent and diagnostic agent for these chronic diseases.